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Neuro Block 4 - KJ > Hypothalamic Control of Eating > Flashcards

Hypothalamic Control of Eating Flashcards

1
Q

Why do we stop eating?

A

Satiety

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2
Q

What signals satiety in the short term?

A

CCIC released in the GI tract!

-Signal sent to brainstem via vagus nerve

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3
Q

What signals satiety in the long term?

A

Fat releases Leptin. This signals to the hypothalamus.
the combined short and long term signals in the brainstem and hypothalamus cause:
-Stop eating & Dec. food intake!

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4
Q

What controls meal size?

A

“Satiety” signals

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5
Q

What short-term signals cause decreased eating?

A
  • Oropharyngeal
  • Gastric distention vs. gastric nutrient satiety
  • Post-absorptive Satiety
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6
Q

What is the oropharyngeal short term signal?

A

Putting food in mouth/taste:

  • Fed state: dec. feeding
  • Fasting state: inc. feeding
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7
Q

What was the Phillips and Powley gastric infusion mouse study?

A

Made mice they could deliver food directly too using pyloric cuff between the stomach and intestines.

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8
Q

What did they find in the gastric infusion study?

A
  1. Gastric stretch –> causes decreased food intake
  2. Gastric nutrients (putting sucrose into the stomach) —> caused no further decrease in food intake
    (nutrient value had no effect, just stretch)
  3. Intestinal nutrients –> Sucrose in the intestines caused —-> decreased food intake
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9
Q

What factors cause pre absorptive satiety?

A
  1. Gastric stretch

2. Intestine nutrients (calories)

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10
Q

What causes post-absorptive satiety?

A 
Liver factors!
The portal vein has sensors:
1. Glucose
2. Free fatty acids
[These both decrease food intake]
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11
Q

How does gastric distention cause changes in the CNS that cause decreased food intake?

A
  1. Causes increased mechanoreceptor activity
  2. These mechanoreceptors cause Inc. in Vagus activity
  3. This information is sent from vagus nerve to NTS (Nucleus Tractus Solitarius - Solitary Nucleus)
  4. The NTS causes decreased food intake
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12
Q

What does leptin do to gastric stretch?

A

Increases responsiveness to gastric stretch/more sensitivity (it takes less food to cause decreased food intake) - Leptin is in the brainstem acting on vagal afferents and solitary (NTS) tract.

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13
Q

What releases CCK (Cholecystokinin) and why?

A

Duodenum, in response to meals

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14
Q

What does CCK act on and what does this pathway cause?

A

It acts on CCK receptors –> inc. stimulation of vagal afferents —> Inc. stimulation in NTS —> Dec. food intake

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15
Q

What does CCK (Cholecystokinin) cause in the body?

A
  1. Inc. gallbladder contraction –> releases bile for fat digestion
  2. Inc. pyloric constriction –> inc. stomach activity –> promotes digestion
  3. Inc. gastric contractions –> inc. stomach activity –> promotes digestion
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16
Q

What releases Gherkin and what does it cause?

A

Released from stomach

  • > It’s increased by fasting
  • > Orexigenic effect: Inc. appetite
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17
Q

What is Prader-Willi syndrome & what are its symptoms?

A 
Deletion on chromosome 15, 1/25,000 
Symptoms: 
-Fetal hypotonia (dec. muscle tone)
-Mental retardation
-Hypogonadotropic hypogonadism (Dec. FSH, Dec. LH --> Dec. gonado function)
-Obesity 
-Hyperphagia (excessive eating)
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18
Q

What hormone is high in Prader-Willi?

A

High blood Ghrelin, which increases appetite

19
Q

What releases Leptin? What type of signal is it?

A

Adipocytes, its a long-term satiety signal

fat stores are controlled by “adiposity” signals

20
Q

What might overweight people have a problem with?

A

Leptin receptors!

21
Q

What is Leptin?

A
  • Ob protein/gene product

- Adipocytes release leptin and it causes Dec. food intake

22
Q

Where does leptin work?

A
  1. Brainstem (NTS)

2. Hypothalamus

23
Q

What is the role of ghrelin again?

A

Inc. food intake!

24
Q

Where does ghrelin act?

A

Inc. NPY neuronal activity within ARC (Arcuate nucleus)

25
Q

Where is the LHA (Lateral Hypothalamic Area)?

A

On the lateral areas/wings of coronal section

26
Q

What happens when you lesion the LHA (lateral hypothalamic area)?

A

Don’t eat/cessation of eating (Aphagia)

27
Q

What causes aphagia in LHA damage?

A
  • Damage to the medial forebrain bundle (part of mess-limbic system) that causes (1) reduced motivation to eat and (2) reduced motor function (axons damaged may be involved in motor control)
  • Loss of neurons that synthesize “orexigenic” peptide
28
Q

What happens when LHA is stimulated?

A

Release of “anabolic” neurotransmitted in the brainstem

—> causes increased eating!

29
Q

What happens when the PVN is activated/stimulated?

A

Activation of PVN –> release of “catabolic - break down” (dec. eating) neurotransmitters in brainstem

30
Q

What does the paraventricular nucleus (PVN) cause?

A

Releases oxytocin & vasopressin from same neurons.

PVN neurons send axons to brainstem to regulate food intake —> Dec. eating

31
Q

What does the ARC (arcuate nucleus) do? What does it have?

A

It integrates information.
It has two populations of neurons:
1. Neuropeptide Y (NPY)
2. Melanocortin (POMC-derived peptide)

32
Q

Where do Neuropeptide Y (NPY) and Melanocortin (POMC-derived peptide) project?

A

PVN and LHA nuclei!

33
Q

What does Neuropeptide Y (NPY) neurons cause?

A

Inc. eating (through projections to PVN & LHA)

34
Q

What does Melanocortin (POMC-derived peptide) cause?

A

Dec. eating (through projections to PVN & LHA)

35
Q

What does Leptin inhibit in the ARC? What does it cause?

A

It inhibits NPY neurons, causing decreased food intake.

36
Q

What does Leptin activate in the ARC? What does it cause?

A

It activates melanocortin activity, causing decreased food intake

37
Q

What does NPY do overall?

A

Inc. Eating

38
Q

What does Alpha-MSH do overall?

A

Melanocortin: Dec. eating

39
Q

What does Leptin do overall?

A

Dec. eating

40
Q

What does CRH do overall?

A

Dec. eating

41
Q

What does Orexin do overall?

A

Inc. eating

42
Q

What does CCK do overall?

A

Dec. eating/motor movement

43
Q

What does Gastric stretch do overall?

A

Dec. eating/motor movement

Neuro Block 4 - KJ (12 decks)

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